Catálogo de publicaciones - revistas

<jats:title>New crustal clues from old rocks</jats:title> <jats:p> The ghost of continental crust long eroded away may exist in certain element ratios found in Archean rocks. Tang <jats:italic>et al.</jats:italic> used Ni/Co and Cr/Zn ratios as a proxy for the magnesium oxide that long ago weathered away in Earth's oldest rocks. This allowed a reconstruction of rock composition, which appears to be very different from that of the crust today. The shift to contemporary crust composition occurred after the Archean era, suggesting the onset of plate tectonics. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6271" page="372" related-article-type="in-this-issue" vol="351" xlink:href="10.1126/science.aad5513">372</jats:related-article> </jats:p>

<jats:title>Let me comfort you</jats:title> <jats:p> Consolation behavior promotes stress reduction of one by another. We know that consolation occurs in humans and apes. Burkett <jats:italic>et al.</jats:italic> observed that within a pair of monogamous prairie voles, an unstressed partner increased its grooming of a stressed partner. Furthermore, the unstressed partner matched the stressed partner in its stress hormone response. Thus, consolation may be more common than assumed in animals, and prairie voles may prove a useful model for understanding the physical and neural mechanisms underlying consolation behavior. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6271" page="375" related-article-type="in-this-issue" vol="351" xlink:href="10.1126/science.aac4785">375</jats:related-article> </jats:p>

<jats:title>Neuronal migrations follow vascular pathways</jats:title> <jats:p> In the developing brain, various types of cells migrate from their birthplaces to their workplaces. Oligodendrocyte precursors, which develop to form the insulating sheaths that make signal transmission along an axon faster, travel farther than many. Tsai <jats:italic>et al.</jats:italic> now show just how the oligodendrocyte precursor cells find their way (see the Perspective by Dejana and Beltsholtz). The progenitor cells follow along the endothelial cells of the vasculature. Disrupting endothelial cells interfered with oligodendrocyte migration, leaving some sections of the brain deficient in insulators. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6271" page="379" related-article-type="in-this-issue" vol="351" xlink:href="10.1126/science.aad3839">379</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6271" page="341" related-article-type="in-this-issue" vol="351" xlink:href="10.1126/science.aaf1139">341</jats:related-article> </jats:p>

<jats:title>Cell death establishes a site for development</jats:title> <jats:p> As plant roots grow through the soil, lateral roots emerge to reach more resources. Xuan <jats:italic>et al.</jats:italic> now show that programmed cell death sets the course for lateral root development. Cells in a specialized region of the root cap periodically die off as a group, defining a location at which a lateral root will later develop. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6271" page="384" related-article-type="in-this-issue" vol="351" xlink:href="10.1126/science.aad2776">384</jats:related-article> </jats:p>

<jats:title>Offspring affected by sperm small RNAs</jats:title> <jats:p> Paternal dietary conditions in mammals influence the metabolic phenotypes of offspring. Although prior work suggests the involvement of epigenetic pathways, the mechanisms remains unclear. Two studies now show that altered paternal diet affects the level of small RNAs in mouse sperm. Chen <jats:italic>et al.</jats:italic> injected sperm transfer RNA (tRNA) fragments from males that had been kept on a high-fat diet into normal oocytes. The progeny displayed metabolic disorders and concomitant alteration of genes in metabolic pathways. Sharma <jats:italic>et al.</jats:italic> observed the biogenesis and function of small tRNA-derived fragments during sperm maturation. Further understanding of the mechanisms by which progeny are affected by parental exposure may affect human diseases such as diet-induced metabolic disorders. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6271" page="397" related-article-type="in-this-issue" vol="351" xlink:href="10.1126/science.aad7977">397</jats:related-article> , p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6271" page="391" related-article-type="in-this-issue" vol="351" xlink:href="10.1126/science.aad6780">391</jats:related-article> </jats:p>

<jats:title>Offspring affected by sperm small RNAs</jats:title> <jats:p> Paternal dietary conditions in mammals influence the metabolic phenotypes of offspring. Although prior work suggests the involvement of epigenetic pathways, the mechanisms remains unclear. Two studies now show that altered paternal diet affects the level of small RNAs in mouse sperm. Chen <jats:italic>et al.</jats:italic> injected sperm transfer RNA (tRNA) fragments from males that had been kept on a high-fat diet into normal oocytes. The progeny displayed metabolic disorders and concomitant alteration of genes in metabolic pathways. Sharma <jats:italic>et al.</jats:italic> observed the biogenesis and function of small tRNA-derived fragments during sperm maturation. Further understanding of the mechanisms by which progeny are affected by parental exposure may affect human diseases such as diet-induced metabolic disorders. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6271" page="397" related-article-type="in-this-issue" vol="351" xlink:href="10.1126/science.aad7977">397</jats:related-article> , p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6271" page="391" related-article-type="in-this-issue" vol="351" xlink:href="10.1126/science.aad6780">391</jats:related-article> </jats:p>

<jats:title>Editing can help build stronger muscles</jats:title> <jats:p> Much of the controversy surrounding the gene-editing technology called CRISPR/Cas9 centers on the ethics of germline editing of human embryos to correct disease-causing mutations. For certain disorders such as muscular dystrophy, it may be possible to achieve therapeutic benefit by editing the faulty gene in somatic cells. In proof-of-concept studies, Long <jats:italic>et al.</jats:italic> , Nelson <jats:italic>et al.</jats:italic> , and Tabebordbar <jats:italic>et al.</jats:italic> used adeno-associated virus-9 to deliver the CRISPR/Cas9 gene-editing system to young mice with a mutation in the gene coding for dystrophin, a muscle protein deficient in patients with Duchenne muscular dystrophy. Gene editing partially restored dystrophin protein expression in skeletal and cardiac muscle and improved skeletal muscle function. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6271" page="400" related-article-type="in-this-issue" vol="351" xlink:href="10.1126/science.aad5725">400</jats:related-article> , p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6271" page="403" related-article-type="in-this-issue" vol="351" xlink:href="10.1126/science.aad5143">403</jats:related-article> , p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6271" page="407" related-article-type="in-this-issue" vol="351" xlink:href="10.1126/science.aad5177">407</jats:related-article> </jats:p>

<jats:title>Editing can help build stronger muscles</jats:title> <jats:p> Much of the controversy surrounding the gene-editing technology called CRISPR/Cas9 centers on the ethics of germline editing of human embryos to correct disease-causing mutations. For certain disorders such as muscular dystrophy, it may be possible to achieve therapeutic benefit by editing the faulty gene in somatic cells. In proof-of-concept studies, Long <jats:italic>et al.</jats:italic> , Nelson <jats:italic>et al.</jats:italic> , and Tabebordbar <jats:italic>et al.</jats:italic> used adeno-associated virus-9 to deliver the CRISPR/Cas9 gene-editing system to young mice with a mutation in the gene coding for dystrophin, a muscle protein deficient in patients with Duchenne muscular dystrophy. Gene editing partially restored dystrophin protein expression in skeletal and cardiac muscle and improved skeletal muscle function. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6271" page="400" related-article-type="in-this-issue" vol="351" xlink:href="10.1126/science.aad5725">400</jats:related-article> , p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6271" page="403" related-article-type="in-this-issue" vol="351" xlink:href="10.1126/science.aad5143">403</jats:related-article> , p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6271" page="407" related-article-type="in-this-issue" vol="351" xlink:href="10.1126/science.aad5177">407</jats:related-article> </jats:p>

<jats:title>Editing can help build stronger muscles</jats:title> <jats:p> Much of the controversy surrounding the gene-editing technology called CRISPR/Cas9 centers on the ethics of germline editing of human embryos to correct disease-causing mutations. For certain disorders such as muscular dystrophy, it may be possible to achieve therapeutic benefit by editing the faulty gene in somatic cells. In proof-of-concept studies, Long <jats:italic>et al.</jats:italic> , Nelson <jats:italic>et al.</jats:italic> , and Tabebordbar <jats:italic>et al.</jats:italic> used adeno-associated virus-9 to deliver the CRISPR/Cas9 gene-editing system to young mice with a mutation in the gene coding for dystrophin, a muscle protein deficient in patients with Duchenne muscular dystrophy. Gene editing partially restored dystrophin protein expression in skeletal and cardiac muscle and improved skeletal muscle function. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6271" page="400" related-article-type="in-this-issue" vol="351" xlink:href="10.1126/science.aad5725">400</jats:related-article> , p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6271" page="403" related-article-type="in-this-issue" vol="351" xlink:href="10.1126/science.aad5143">403</jats:related-article> , p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6271" page="407" related-article-type="in-this-issue" vol="351" xlink:href="10.1126/science.aad5177">407</jats:related-article> </jats:p>